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Titolo:
Analysis of the p53 tumor suppressor gene in rheumatoid arthritis synovialfibroblasts
Autore:
Kullmann, F; Judex, M; Neudecker, I; Lechner, S; Justen, HP; Green, DR; Wessinghage, D; Firestein, GS; Gay, S; Scholmerich, J; Muller-Ladner, U;
Indirizzi:
Univ Regensburg, Dept Internal Med 1, D-93042 Regensburg, Germany Univ Regensburg Regensburg Germany D-93042 , D-93042 Regensburg, Germany La Jolla Inst Allergy & Immunol, La Jolla, CA USA La Jolla Inst Allergy & Immunol La Jolla CA USA mmunol, La Jolla, CA USA Univ Calif San Diego, Sch Med, La Jolla, CA 92093 USA Univ Calif San Diego La Jolla CA USA 92093 ch Med, La Jolla, CA 92093 USA Univ Zurich Hosp, CH-8091 Zurich, Switzerland Univ Zurich Hosp Zurich Switzerland CH-8091 CH-8091 Zurich, Switzerland
Titolo Testata:
ARTHRITIS AND RHEUMATISM
fascicolo: 8, volume: 42, anno: 1999,
pagine: 1594 - 1600
SICI:
0004-3591(199908)42:8<1594:AOTPTS>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
CONFORMATION POLYMORPHISM ANALYSIS; SEVERE COMBINED IMMUNODEFICIENCY; CELL-LINES; GEL-ELECTROPHORESIS; UPDATED COMPILATION; MUTATIONS; OVEREXPRESSION; APOPTOSIS; CANCER; SENSITIVITY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Muller-Ladner, U Univ Regensburg, Dept Internal Med 1, D-93042 Regensburg,Germany Univ Regensburg Regensburg Germany D-93042 urg, Germany
Citazione:
F. Kullmann et al., "Analysis of the p53 tumor suppressor gene in rheumatoid arthritis synovialfibroblasts", ARTH RHEUM, 42(8), 1999, pp. 1594-1600

Abstract

Objective. To determine whether mutations in the tumor suppressor gene p53may contribute to the transformed-appearing phenotype of rheumatoid arthritis (RA) synovial fibroblasts. Methods, We performed p53 gene mutation analysis using different molecularapproaches. Synovial fibroblasts of 10 patients with RA were cultured and RNA and DNA were harvested after 3-5 passages in cell culture. Sequence analysis of all exons of the p53 gene was performed using 3 different techniques: 1) single-strand conformational polymorphism, 2) nonisotopic RNase cleavage assay, and 3) base excision sequence scanning T-scan, followed by sequence analysis of specific gene segments. Results. Although p53 antigen could be detected by immunocytochemistry in numerous cultured fibroblasts, gel electrophoresis analysis of products obtained using all 3 methods and subsequent sequence analysis showed no specific mutation pattern in the genome of the synovial fibroblasts from patientsin Germany, including the known "hot spots" within the p53 genome. However, p53 mutations were identified in different clones of 3 additional Ri synovial fibroblast populations from the United States. Sequence analysis of the p53 promoter did not reveal mutational base changes. Conclusion, The findings of the study support the hypothesis that the majority of the mutations of the p53 gene observed in RA synovium are not derived from the genome of RA synovial fibroblasts, and that the variability of the mutation pattern reflects, in part, the heterogeneity of the disease.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/03/20 alle ore 15:34:52